Significant decrease of adiponectin plasmatic levels following two different programs of resistance training in healthy and well-trained young adults

Adiponectin is a hormone secreted by adipose tissue that exerts a pleiotropic effect on many tissues and organs, including skeletal muscles, bones, liver, and brain, regulating energy balance, insulin sensitivity, and inflammation processes (1,2). This adipokine is secreted into circulation in three different oligomeric forms: trimers, hexamers, and high-molecular-weight (HMW) oligomers. The HMW form is the most active in the regulation of body weight and energy balance (3). Adiponectin plays a key role in metabolic adaptation induced by physical exercise (4,5). While its regulation after aerobic exercise has been widely investigated, less is known about its short-term modulation after strength training in healthy subjects. In this study, nine resistance-trained young men have been enrolled to perform two different sessions of total-body resistance exercises. The first training session (ETS1) was characterized by high time under tension TUT (5-1-2-1 cadence, to failure), emphasizing the eccentric phase of the movement, while the second (ETS2) had moderate TUT (2-1-2-1 cadence, two repetitions in reserve), representing a traditional submaximal resistance training protocol. Adiponectin concentration was assessed by ELISA in plasma and saliva samples collected before exercise (baseline), upon 15 minutes, 24 and 48 hours of both training sessions. Muscle soreness, plasma creatine kinase (CK) and a visual analog scale (VAS) were also measured. Plasma adiponectin decreased significantly following both training sessions of approximatively 15-20% upon 24h and reaching 25% of decrease 48 hours post-exercise (P<0.001). No significant difference of circulating adiponectin levels was detected between ETS1 and ETS2 sessions. Western blot analyses confirmed a decrease in plasma levels of adiponectin, especially HMW oligomers. Salivary adiponectin remained unchanged following both training sessions. Correlation analyses revealed an inverse association between adiponectin and CK during recovery period. Overall, the two sessions of strength training induced a transient and rapid reduction of circulating adiponectin, independent form exercise modality, suggesting an activation of adiponectin signaling determined by acute metabolic stress. This hormone may contribute to inflammatory response during the subsequent recovery phase to repair muscle damage. Moreover, the dissociation between plasma and salivary levels of adipokine indicates its complex regulation. These findings extend existing knowledge on adiponectin and its modulation upon strength training and its potential role in metabolic homeostasis.